"People consuming at least 20 grams of nuts daily less likely to develop potentially fatal conditions such as heart disease and cancer," The Independent reports. That was the main finding of a review looking at 20 previous studies on the benefits of nuts.

Researchers found consistent evidence that a 28 gram daily serving of nuts – which is literally a handful (for most nuts) – was linked with around 20% reduced risk of heart disease, cancer and death from any cause.

However, as is so often the case with studies into diet and health, the researchers cannot prove nuts are the sole cause of these outcomes.

It's hard to discount the possibility that nuts could be just one component of a healthier lifestyle pattern, including balanced diet and regular physical activity. It could be this overall picture that is reducing risk, not just nuts.

The researchers tried to account for these types of variables, but such accounting is always going to be an exercise in educated guesswork.

Also, many non-lifestyle factors may be involved in any individual's risk of disease. For example, if you are a male with a family history of heart disease, a healthy diet including nuts can help, but still may not be able to eliminate the risk entirely.

The link between nuts and improved health is nevertheless plausible. As we pointed out during a discussion of a similar study in 2015: "Nuts are a good source of healthy unsaturated fats, protein, and a range of vitamins and minerals … Unsalted nuts are the healthiest option."

Where did the story come from?

The study was carried out by researchers from Norwegian University of Science and Technology, Trondheim, Norway, Imperial College London, and other institutions in the US.

It was funded by Olav og Gerd Meidel Raagholt's Stiftelse for Medisinsk forskning (a Norwegian charitable foundation), the Liaison Committee between the Central Norway Regional Health Authority and the Norwegian University of Science and Technology (NTNU), and Imperial College National Institute of Health Research (NIHR) Biomedical Research Centre (BRC).

What kind of research was this?

Previous studies have suggested an intake of nuts is beneficial, and some have found it could be linked with reduced risk of cardiovascular disease and cancer. Other studies though have found no link. The researchers consider the possibility that there is a weak link and that's what they aimed to look at.

A systematic review is the best way of compiling all literature on a topic available to date. However, systematic reviews are only as good as the underlying evidence. Studies looking at dietary factors are often observational and it is difficult to rule out the possibility of confounding variables from other health and lifestyle factors.

What did the researchers do?

The researchers searched two literature databases to identify any randomised controlled trials (RCTs) or prospective cohort studies that had looked at how nut intake in adults was linked with cardiovascular disease, cancer and death from any cause.

Studies had to report information on nut intake specifically (ideally by dose and frequency). Researchers assessed the quality of studies for inclusion.

Twenty prospective cohort studies met the inclusion criteria. Nine studies came from the US, six from Europe, four from Asia, and one came from Australia. All studies included adult populations; five were in women only, three in men only, and 12 in a mixed population.

The researchers did not find any suitable RCTs to include in their analysis. This is not especially surprising as RCTs involving diet are notoriously difficult to carry out. You could never be sure that everyone who was randomised into the "eat no nuts" group would stick to the plan, or vice versa.

Also they'd need large samples and long follow-up times to capture disease outcomes, so are not usually feasible.

This was for any nut intake, but risk reductions were also found when analysing peanuts or tree nuts separately. Increasing intake was associated with reduced risk up to 15grams/day, above which there was no further risk reduction.

Cancer

Nine cohorts (304,285 adults) found that one serving of nuts per day reduced risk of any cancer by 15% (RR 0.85, 95% CI 0.76 to 0.94). By separate analysis, the risk reduction was slightly higher for tree nuts (20%) than peanuts (7%).

All-cause death

Fifteen cohorts (819,448 people) recorded 85,870 deaths. One serving of nuts a day was linked with a 22% reduced risk of death during study follow-up (RR 0.78, 95% CI 0.72 to 0.84).

Looking at specific causes of death, each serving of nuts a day was linked with reduced risk of respiratory deaths (0.48 (0.26–0.89); three studies) and diabetes deaths (RR 0.61, 0.43 to 0.88; four studies).

There was no link with deaths from neurodegenerative diseases, and inconsistent links with deaths from kidney disease and infectious diseases. No other disease-related causes were reported.

Overall, the researchers estimate that 4.4 million premature deaths in 2013 across America, Europe, Southeast Asia and Western Pacific could be attributable to nut intakes below 20 grams/day.

What did the researchers conclude?

The researchers conclude: "Higher nut intake is associated with reduced risk of cardiovascular disease, total cancer and all-cause mortality, and mortality from respiratory disease, diabetes, and infections."

Conclusions

This systematic review finds evidence that nut intake may be linked with reduced risk of cardiovascular disease, cancer and death.

The systematic review has several strengths. It identified a large number of studies with a large total sample size. It also included only prospective cohorts assessing nut consumption and then followed up later disease outcomes.

It excluded cross sectional studies, which assess diet and disease at the same time, and so can't show the direction of effect. It also excluded cohorts that have retrospectively questioned diet when the person already has the disease, which could be subject to recall bias.

However, there are still a number of inherent limitations which mean these studies cannot easily prove that nuts are the magic dietary ingredient that are solely and directly responsible for these outcomes.

There were no randomised controlled trials of nut consumption. All studies were observational where people were choosing their own diet.

The researchers took care to include studies that only looked at nut consumption as an independent factor and looked at results that had adjusted for any confounders. However, the factors that the studies adjusted for, and how well they were assessed, will have varied across studies.

As such it's very difficult to prove that nuts alone are the causative factor and they are not just one component of a generally healthier lifestyle pattern, including balanced diet, regular physical activity, not smoking, and moderating alcohol.

When it comes to frequency or quantity of intake, it is likely there is an element of inaccuracy when people report how much they eat. For example, most people wouldn't weigh out how many nuts they're eating each day.

The review also provides limited information about specific types of nuts. Considering peanuts in particular, the studies included in the review didn't specify whether these are plain nuts, or whether they could have added salt and oils.

It is also likely that cardiovascular and cancer outcomes were not assessed the same way in all studies, for example whether by participant self-report or by checking medical records.

Overall there does seem to be a link between nut consumption and health, but nuts alone won't reduce your risk of cardiovascular disease or cancers, if your lifestyle is still generally unhealthy.

"Swapping butter and meat for olive oil and fish does cut the risk of heart disease," The Times reports.

The headline is prompted by the findings from a US study involving data from over 100,000 men and women, followed for more than 20 years. The results showed that consumption of different types of saturated fats was associated with an increased risk of coronary heart disease.

The researchers also found that replacing just 1% of energy consumed in the form of saturated fats with polyunsaturated fats, monounsaturated fats, wholegrain carbohydrates or plant proteins, led to a 5-8% decreased risk of coronary heart disease.

The debate regarding the risks of "sat fats" continues.

A report we discussed in May this year argued that the current UK guidelines on saturated fats were flawed as there was no proven link between saturated fat consumption and heart disease. But critics attacked the report for lacking independent peer review. The British Heart Foundation said it did not offer enough evidence to "take it seriously".

Current guidelines recommend that men eat no more than 30g of saturated fat a day and women no more than 20g of saturated fat, and this latest research appears to support current guidelines.

Where did the story come from?

The study was carried out by researchers from Harvard T.H. Chan School of Public Health, US and the Unilever Research & Development institute in the Netherlands. It was funded by the National Institutes of Health and the National Heart, Lung and Blood Institute and supported by Unilever. The study was published in the peer-reviewed British Medical Journal on an open-access basis, so it is free to read online.

One author declares they are supported by a grant from Unilever Research & Development and three other authors are employees of Unilever Research & Development. Unilever is a producer of food consumer products and as such there may be a conflict of interest.

Generally the UK’s media reported the story accurately.

However, the Daily Mail suggests that the fats identified in the study as increasing risk of coronary heart disease "be replaced in diets by other food like carbohydrates".

This may be misleading, as food products perceived by the public as carbohydrates may also contain ingredients such as butter that are high in saturated fats. The study only looked at wholegrain carbohydrates as a replacement for these fats.

What kind of research was this?

This was a longitudinal cohort study, which recruited male and female health professionals and followed them for over 20 years to assess how proportions of saturated fatty acids in the diet might affect risk of coronary heart disease later on.

This type of study is useful for suggesting links between factors but cannot prove that one factor – saturated fat intake – causes another – coronary heart disease.

The researchers tried to control for confounding factors, but there may be unmeasured factors, such as stress, that affect risk of coronary heart disease.

What did the research involve?

Researchers used data from the Nurses' Health Study, which included 73,147 female nurses and a cohort of 42,635 men from the Health Professionals Follow-up Study.

Information was collected at study baseline (1984 in the Nurses' Study and 1986 in the Health Professionals Study) on medical history, lifestyle, potential risk factors and disease diagnosis.

Participants also completed a food frequency questionnaire at baseline and then every four years until 2010, in which participants were asked how often they consumed specific foods in the previous year, ranging from "never" to "at least six per day". Cumulative averages of food intake were calculated from all dietary questionnaires completed in the follow-up.

Saturated fatty acids were distinguished by the length of their carbon chain. The number on the left indicates the number of carbon atoms and the number on the right the number of double bonds (saturated fatty acids do not have any double bonds). Therefore lauric acid (12:0) has 12 carbon atoms with no double bonds.

The major fatty acids included in the analysis were:

lauric acid (12:0), found in high quantities in coconut and palm kernel oils

Age-adjusted intake of individual saturated fatty acids was calculated and risk of non-fatal and fatal coronary heart disease was determined. The researchers adjusted their results to take into account the following possible confounding factors:

ethnicity

family history of myocardial infarction (heart attack)

body mass index

cigarette smoking

alcohol intake

physical activity

multivitamin use

menopausal status

postmenopausal hormone use

current aspirin use

baseline hypertension

baseline hypercholesterolemia

total energy intake

What were the basic results?

All participants were free of chronic illness at the beginning of the study. During the follow-up period, 7,035 cases of coronary heart disease were identified (4,348 were non-fatal; 2,687 were fatal).

Higher consumption of one type of fatty acid was associated with higher consumption of all fatty acids analysed.

Comparing groups with the highest and lowest intake of individual saturated fat intakes, there was an increased risk of coronary heart disease of:

There was no significant decrease when replaced by monounsaturated fat (HR 1.05, 95% CI 0.90 to 1.01)

Participants who consumed higher proportions of saturated fatty acids were also more likely to be white, non-smokers, engage in less physical activity, less likely to take multivitamins and have a higher intake of total energy.

How did the researchers interpret the results?

The researchers concluded that "dietary replacement of 12:0-18:0 with more healthy macronutrients – such as polyunsaturated fat and wholegrain carbohydrates – was associated with a lower risk of coronary heart disease".

They further add that "owing to high correlations among individual saturated fatty acids (SFAs) in diet, these findings support the current dietary recommendations that focus on replacement of total saturated fat as an effective approach to preventing cardiovascular disease. The public health and clinical significance of modulating the content of individual SFAs in specific foods should be further evaluated".

Conclusion

This study shows an association between increased intake of individual saturated fats and increased risk of coronary heart disease.

It also shows a link between the replacement of these fatty acids with other types of fat, plant protein, or wholegrain carbohydrates and a reduction in coronary heart disease risk.

The strengths of this study are the large sample size and long follow-up period that looked at repeated measures such as diet, lifestyle and health outcomes.

It also provides clear support for dietary guidelines that recommend replacing dietary energy from saturated fats with polyunsaturated fats as well as wholegrain carbohydrates and plant source proteins.

However, there are a number of limitations to the study:

Although the study adjusted for confounding variables, there may be other factors that were not accounted for. For example, stress and life events might be contributors to coronary heart disease, but were not measured.

The analysis was based on self-reported dietary intake and therefore may be subject to recall bias.

The study populations were comprised of health professionals who might have very similar lifestyles to one another; therefore the results may not be representative of other populations.

Finally, most people did not just eat only one type of saturated fat, so it is hard to disentangle which have more association with coronary heart disease.

Also, the study did not consider other types of fatty acids, such as those found in dairy products, that may have beneficial effects.

There is ongoing controversy about how much of a threat saturated fats do actually pose to health.

Current UK government guidelines advise cutting down on all fats and replacing saturated fat with some unsaturated fat. Read more advice about fats

They also recommended that people at risk of having low vitamin D levels should take supplements all year round.

The public health body was concerned that a combination of limited sunlight exposure – which stimulates the production of vitamin D – and a diet low in vitamin D may contribute to very low vitamin D levels, known as deficiency, in some people.

Vitamin D deficiency can lead to a range of complications, including a condition called osteomalacia, which makes bones soft, painful and more likely to break.

What is the basis for these current reports?

Researchers from the University of Auckland and the University of Aberdeen published a review in the BMJ that questions the evidence of PHE's recommendation about vitamin D supplements.

The researchers say that, despite much good-quality research into vitamin D, there is no evidence that taking vitamin D supplements alone reduces the risk of fractures or falls, or improves bone strength.

They say two studies into giving vitamin D supplements with calcium, which involved elderly women with very low vitamin D levels living in care homes, did show a reduction in fractures.

But studies in people who did not live in care homes did not find the same results.

The authors also looked at reports of other possible benefits of vitamin D, apart from bone and muscle health, and found "no consistent effect" of benefits.

As the authors of the review did not outline their search strategy for their evidence, it should be considered a narrative review (where researchers highlight evidence supporting their argument) rather than a systematic review (where researchers consider all available appropriate evidence).

A systematic review is considered to have more "weight of evidence".

The BMJ also included a "right of reply" piece by Dr Louis Levy, head of nutrition science at Public Health England.

Dr Levy makes the point that, "Vitamin D is found in only a small number of foods, including oily fish, red meat, liver and egg yolk, so it's not easy to get what you need from your diet alone."

"People with darker skin, from African, Afro-Caribbean, and south Asian backgrounds, may not get enough vitamin D from sunlight in the summer and should also consider taking a supplement all year round."

Most experts agree that people who are at high risk of low vitamin D levels may benefit from taking vitamin D supplements.

What is vitamin D deficiency?

Vitamin D is important for building healthy bones and muscles. Severe vitamin D deficiency can cause malformed bones (rickets) in children and osteomalacia in adults.

However, there's much scientific debate about what is considered a vitamin D deficiency and how much we need daily.

In July, PHE said everyone should aim to have a dietary intake of 10mcg of vitamin D daily, as it was difficult to say how much vitamin D is made by sunlight on skin.

Most of our vitamin D is made by sunshine on our skin. But in winter, sunlight in the UK is thought to be too weak to allow our skin to make vitamin D.

There's also vitamin D in some food – including oily fish like salmon, mackerel, herring and sardines, and red meat and eggs – as well as some breakfast cereals and fat spreads that have vitamin D added to them.

How does vitamin D affect you?

If you're not at high risk of a vitamin D deficiency, you probably get enough from a combination of food and sunshine during the summer months.

PHE says adults should "consider" taking a daily supplement of 10mcg in the autumn and winter. The authors of the BMJ paper say this recommendation is unnecessary for most people.

But 10mcg is unlikely to be harmful, so it's a matter of individual choice. You should check that you're not taking vitamin D in multivitamin supplements as well.

Certain groups of people may be at higher risk of having a vitamin D deficiency:

people who don't go outside very often – for example, those who live in care homes

people who cover most of their skin when outside

people with darker skin from African, Caribbean and south Asian backgrounds

PHE recommends these groups consider taking a supplement all year round. They also recommend daily supplements for pregnant women, babies and children aged four years old or younger.

Conclusion

So, who's right? The authors of the BMJ review are certainly correct in their argument that, ideally, we can get all the vitamin D we need through a combination of diet and sensible exposure to sunlight.

They are also right that the evidence does not show that people with normal levels of vitamin D benefit from taking supplements.

But we don't live in an ideal world. The truth is many people in the UK eat unhealthy, vitamin D-poor diets and also don't get enough exposure to sunlight.

A sensible approach would be to consider taking vitamin D supplements as recommended, but also be alert for possible signs of excessive vitamin D levels causing a build-up of calcium in the blood (hypercalcemia).

Warning signs and symptoms of hypercalcemia include loss of appetite, feeling and being sick, and needing to pee frequently.

"Bagged salad can fuel the growth of food-poisoning bugs like salmonella and make them more dangerous," BBC News reports.

Researchers found evidence that the environment inside a salad bag offers an ideal breeding ground for salmonella, a type of bacteria that is a leading cause of food poisoning.

They grew salmonella in salad juice and leaves at different temperatures to see what happened, and found salad leaf juice – released from the leaves when they're damaged or broken – supports the growth of salmonella, even at fridge temperature.

They also found that if leaves are contaminated, the bacteria aren't removed by washing in water.

However, the chances of a salad bag being contaminated by salmonella or other bacteria in the first place are thought to be low.

An independent expert commented: "The rates of produce that have been found to be contaminated are between 0-3%."

That said, it is important not to be complacent. An E. coli outbreak in July this year, thought to be linked to contaminated salad, killed two people and hospitalised 62 others.

You should wash your hands thoroughly with soap and water, then dry them carefully, after using the toilet and before eating or preparing food.

You should also wash fruit and vegetables before eating them – although washing did not remove salmonella in this study – and pay attention to use-by dates.

The UK media's reporting was accurate, but some of the headlines could imply that salad bags have suddenly been found to be contaminated with salmonella: they haven't.

The potential for contamination is nothing new and something that the food industry tries to guard against.

What the study shows is that if salmonella is present, it will quickly grow to levels that could trigger food poisoning, even if the salad bag is placed in a fridge.

What kind of research was this?

This laboratory study aimed to examine the "behaviour" of salmonella bacteria if present in a bag of salad leaves.

Consumption of salad leaves like lettuce and spinach has increased considerably in recent years.

But they are highly perishable and require rapid processing and special packaging to keep them fresh.

They are particularly at risk of colonisation from the gut microbes E. coli, salmonella and listeria.

These may be present in contaminated soil or be transferred during the various processes of trimming, washing, packaging and transport, or through contaminated water or poor hygiene among people involved in food production.

The potentially contaminated leaves are usually eaten raw, which doesn't give any further opportunities to eradicate the bacteria through cooking, for example.

Salad leaves are said to be ranked as the second most common source of outbreaks of foodborne illness.

This study aimed to look at the factors that could enhance the growth of bacteria present in salad – for example, the effects of opening the bag or storing it at room temperature.

What did the research involve?

The laboratory tests involved a variety of salad juices, which were prepared by crushing and mixing cos lettuce, baby green oak lettuce, red romaine, spinach and red chard – each obtained from a selection of pre-prepared bagged salads.

The researchers conducted a series of tests. In one experiment, they put salmonella cultures into a fluid medium and incubated salad leaf juice in this fluid for 18 hours at 37C (98.6F).

To model what may happen in a salad bag, they also cultured salmonella in sterile water mixed with 2% leaf juices and refrigerated this at 4C (39.2F) for five days.

The researchers also looked at the growth on salad leaves by mixing salmonella with sterile water, 2% leaf juice and three spinach leaf pieces.

These were incubated at room temperature for 30 minutes, after which the leaves were washed in sterile water.

The researchers similarly tested growth on plastic salad bags and looked at the effect of washing.

What were the basic results?

As would be expected, the researchers found that when they incubated the mix of salmonella, water and leaf juice at the high 37C temperature, salmonella grew on all varieties of leaf juice.

Even though the 4C temperature restricted growth, the bacteria still grew in number over the course of five days in the fridge.

Higher concentrations of leaf juice fluid further increased growth, suggesting the bugs may be able to use the leaf nutrients leached into the bag to support their growth.

This happened with increased concentration of any of the leaf juices, but spinach seemed to have the strongest effect.

The researchers also found salmonella attached to both the plastic bag and the salad leaves. The presence of salad juice increased the ability of salmonella to colonise both of these surfaces.

The bacteria attachment to salad leaves was resistant to several washings in water.

How did the researchers interpret the results?

The researchers say their results show that, "exposure to salad leaf juice may contribute to the persistence of salmonella on salad leaves, and strongly emphasises the importance of ensuring the microbiological safety of fresh produce".

Conclusion

This laboratory study principally demonstrates that salad leaf juice – released from salad leaves when they are damaged or broken – supports the growth of salmonella bacteria, even at fridge temperature. If leaves are contaminated with salmonella, this isn't removed by washing in water.

The results don't show that all packaged salad leaves are contaminated with gut bacteria like salmonella.

What they do show is that if the bags have been contaminated with gut bacteria, these bacteria will replicate, even in the fridge, and there's little you can do to remove them.

The best thing to do is to throw the bag out, although there's no way of knowing whether a particular bag is contaminated or not.

The study also cannot tell us whether we may be safer buying packaged salads unwashed, washed in spring water, or washed in chlorinated water.

And neither can it tell us whether we may be safer buying non-packaged lettuce – it's still possible that an unpacked lettuce may have been contaminated at some point along the line.

"Probiotics found in yoghurt and supplements could help improve thinking and memory for people with Alzheimer's disease," The Daily Telegraph reports after a small study found people given the bacterial supplement had improved scores on brain function tests.

Probiotics are live bacteria and yeasts promoted as having various health benefits, and are often added to yoghurt.

An Iranian research team gave people with severe Alzheimer's disease a probiotic drink every day for 12 weeks, and then measured the changes in brain function test scores before and after the treatment.

They found small improvements after the probiotics were given compared with the placebo group, but it is unclear if these improvements were enough to be clinically useful or noticeable.

While the results are far from conclusive, they do add to a previous body of research that suggests there may be an association between gut health and brain function.

Exploring this association could lead to new insights and possible treatments for Alzheimer's and other forms of dementia.

There are no known safety concerns about probiotics. But based on the small size and short-term nature of this study, more rigorous research would be required before probiotics could be recommended as an evidence-based treatment for people with Alzheimer's disease.

Where did the story come from?

This Iranian study was carried out by researchers from Kashan University of Medical Sciences in Iran and was funded by a grant from the same university.

What kind of research was this?

It also investigated the effect of probiotics on biomarkers for inflammation and metabolism in the body.

Probiotics are often referred to as "good" or "friendly" bacteria, and are found in yoghurts and other dairy products.

Although probiotics have traditionally been recommended for people with gut conditions such as irritable bowel syndrome (IBS), recent research has shown they may benefit the brain, too.

This is because there may be a link between the gut and the brain along what's known as the micro biota-gut-brain axis.

This axis is a biochemical signalling pathway that runs between the brain and the digestive system. But its full role in terms of health outcomes is thought by many to not be fully understood.

Double-blind randomised controlled trials like this one are thought to be the gold standard when it comes to investigating a potential association between an exposure and an outcome – in this case, between probiotic supplements and changes in cognitive function.

What did the research involve?

This 12-week trial recruited 60 patients with Alzheimer's disease with a mean age of 80. The participants were all matched for disease severity based on gender, age and body mass index (BMI).

They were then randomly assigned to two treatment groups (30 participants in each): the control group received plain milk, while the intervention group received probiotic milk (200ml a day).

The patients' cognitive function was measured before and after the 12-week trial using a Mini-Mental State Examination (MMSE). This scale is a 30-point questionnaire used extensively to measure cognitive impairment.

The test takes about 10 minutes to complete and assesses cognitive – or thinking – abilities such as attention, calculation, recall, language, and the ability to follow simple commands.

One example question is to ask people to count backwards from 100 in sevens. Any score greater than or equal to 24 points out of 30 indicates normal cognition.

Blood samples were also collected to assess levels of biomarkers for oxidative stress, which is an indicator of cell damage, as well as inflammation and metabolic profiles.

During the study, four patients from each treatment group died from old age. A total of 52 patients went on to complete the study. The data from these 52 patients was analysed and the findings were compared between the two treatment groups.

What were the basic results?

Overall, the 12-week treatment with probiotic supplements resulted in an improvement in the MMSE score of +27.9%, compared with a decrease of -5.03% in the control group.

In absolute terms this means that the control group deteriorated from 8.47 to 8.00, remaining severely impaired on the 30-point scale. Those taking probiotics improved from 8.67 to 10.57.

Although the difference was statistically significant, it is still a small change and suggests that even after taking probiotics everyone remained severely cognitively impaired.

The probiotic treatment also had a positive influence on a range of other blood markers that were of interest to the researchers.

However, changes in biomarker levels for oxidative stress, fasting plasma glucose (a marker of insulin sensitivity) and other lipid (fat) profiles remained insignificant.

It is not clear if these have a bearing on the development of Alzheimer's and how any link between them and drinking probiotics might be acting.

How did the researchers interpret the results?

The researchers concluded that, "The current study demonstrated that the probiotic administration for 12 weeks has favourable effects on MMSE score, MDA, hs-CRP, markers of insulin metabolism and triglycerides levels of the AD patients; however, the changes in other biomarkers of oxidative stress and inflammation, FPG and other lipid profiles are negligible."

Conclusion

It also investigated the effect of probiotics on biomarkers for inflammation and metabolism in the body.

It found treatment with probiotic supplements resulted in a small improvement in cognitive function compared with the control group.

But everyone remained severely cognitively impaired, and it's not clear if the change in score was clinically important in terms of function.

Although these are interesting findings, there are a few things to bear in mind:

This was a small trial involving 60 people. This intervention would need to be tested on a larger sample size to confirm the findings, as it's still possible that the change observed is a chance finding.

The participants were mainly female – only 12 male patients were involved – and everyone had severe dementia at the start of the study, so it's unclear whether probiotics are able to prevent dementia in the general population.

The trial was conducted for 12 weeks. As Alzheimer's is a progressive disease, it would be beneficial to monitor the long-term effects of probiotics in patients with Alzheimer's disease to know whether the improvement in cognitive function would last longer than three months.

The participants in the trial were an average age of 80. It would be interesting to see if the same effect was observed in patients at an earlier stage of Alzheimer's disease.

Dietary advice for people with Alzheimer's disease is the same for most other people – to eat a healthy, balanced diet.

The researchers divided the mice into three groups: two received emulsifiers, either sodium carboxymethycellulose (CMC) or polysorbate 80 (P80), and the third group received water. They also gave the mice toxins to trigger inflammation and cancer.

Overall, they found more and bigger cancerous tumours in mice given the emulsifiers, in addition to some inflammatory changes. It was suggested the reason could be that emulsifiers altered the balance of gut bacteria, creating an environment more favourable to the development of cancer.

But while these findings may be alarming, it's too early to say if they apply to humans. Findings of animal studies aren't directly transferable to humans. The mice were also given far greater doses of emulsifiers than a human would consume, in addition to toxins that cause inflammation and cancer.

It is well known that bowel cancer is linked to high levels of body fat and eating lots of processed meat, but the link with emulsifiers needs further research.

All food additives undergo a safety assessment before they can be used and it's not yet possible to say for certain whether any of these pose a risk of cancer in humans at the levels permitted.

Where did the story come from?

The study was carried out by researchers from Georgia State University in Atlanta and was funded by a National Institutes of Health (NIH) grant.

The study was published in the peer-reviewed medical journal Cancer Research.

It has largely been reported accurately in the media, which for the most part did mention the limitations of the research.

The Sun provided a quote from Professor Sanders from Kings College London who said the mice were fed the E numbers at a level of 1%, described as: "a very high intake of the food additives compared to what might be found in human diets".

He added: "We can't assume this study is applicable to humans, so it shouldn't be cause for concern."

But some headlines oversimplified the research and implied that a definite link between additives and bowel cancer in humans had been found. Moreover, some of the coverage didn't mention the study's important limitations.

What kind of research was this?

This was an animal study in mice that aimed to see whether food additives (E numbers) called emulsifiers found in processed food could be responsible for bowel cancer.

Emulsifiers prevent foods from separating and give food body and texture. They're commonly found in food such as ice cream.

The researchers suggested that emulsifiers may cause low grade inflammation in the gut and increase levels of bad gut microbes, resulting in increased levels of cancer.

This kind of research is a valuable first step in understanding the processes by which emulsifiers may lead to inflammation in the gut, and then seeing whether this could be linked with cancer risk.

But this is early, animal based research and we can't be sure whether the findings would be the same in humans.

What did the research involve?

The researchers split mice into three groups, with each group being given one of the following:

sodium carboxymethycellulose (CMC) – a soft and lubricating "gum" found in products like ice cream and toothpaste

polysorbate 80 (P80) – a thickening liquid, also found in things like ice creams and sauces to stop them separating

The mice received these solutions for 13 weeks during which time they had their bodyweight measured and faeces collected on a weekly basis.

Following the 13 week period, the mice were given an injection of azoxymethane (AOM), a strong cancer-causing substance in rodents, to induce colon cancer. Five days later a dose of dextran sulfate sodium (DSS) used to induce colitis (inflammation of the lining of the colon).

Five days later they were given a dose of dextran sulfate sodium (DSS) used to induce colitis (inflammation of the lining of the colon).

At the end of the experiment, the mice were killed, and colon length, colon weight, spleen weight and body fatness were measured. Any cancerous tumours found were counted and measured.

What were the basic results?

The mice receiving CMC and P80 showed a small but significant increase in their body mass. The emulsifier treatment also impaired blood glucose regulation. This was evident from increased food consumption and poor fasting blood glucose levels.

All mice receiving AOM and DSS lost weight during DSS treatment. When examined after death they had features of inflammation, including increased colon and spleen weights.

The mice in the two groups given emulsifiers were found to have more inflammatory changes compared to mice in the control group. There was also increased tumour development in the mice that consumed emulsifiers in comparison to the control group.

Further exploration suggested that the greater inflammatory changes and cancer development in the emulsifier groups were caused by these substances altering the balance of gut bacteria.

How did the researchers interpret the results?

The researchers conclude: "We found that emulsifier induced alterations in the microbiome were necessary and sufficient to drive alterations in major proliferation and apotosis [cell death] signalling pathways thought to govern tumour development."

Conclusion

The findings suggest emulsifiers could lead to greater inflammation and bowel cancer in mice, and this may be caused by them altering the balance of gut bacteria. But there are important limitations to note:

The mice were fed large doses of the substances not comparable to the levels found in food humans would eat.

The mice were also given strong drugs both to cause cancer and trigger bowel inflammation. Without these substances, the emulsifiers alone may have had minimal effect.

Findings of animal studies aren't directly transferable to the effect that may be seen in humans consuming food products containing emulsifiers. Human studies would be needed to confirm these findings. For example, researchers could analyse the effect of directly adding emulsifiers to bowel tissue samples in the laboratory.

It's difficult to understand the biological processes that may be behind the increased cancer development in mice exposed to emulsifiers. For example, they may be due to increased weight gain or poor glucose control, rather than the substances being the direct cause.

It's too early to apply these findings to humans. While it's well known that bowel cancer is linked to high levels of body fat and higher consumption of processed meats, the link with emulsifiers is one that needs to be researched further.

"An egg a day can cut chances of suffering a fatal stroke," The Times reports. A new review of existing data covering around 300,000 people suggests eating up to one egg a day may lower stroke risk; but not the risk of heart disease.

The health effects of eggs have been debated for years. Eggs, which contain cholesterol, were thought to increase risk of heart disease by raising cholesterol levels.

But more recent studies show that cholesterol in food has little impact on the levels of cholesterol in your blood – most cholesterol in the blood is made by the liver.

Researchers wanted to carry out an updated analysis of the evidence on the link between eating eggs and the risk of stroke and heart disease.

The analysis found no link with heart disease and a small reduced risk (12%) of stroke for people who ate around one egg a day, compared to those who ate less than two a week.

The research supports the idea that eggs can be part of a healthy diet. However, it didn't look at people's whole diet, so we don't know what else they were eating, or how the eggs were prepared.

Also, the researchers didn't find that more was better – there was no evidence that people reduced their risk in line with the number of eggs they ate.

Eggs are a good source of protein, vitamins and minerals, so adding one a day to your breakfast could be a healthy way to start the day.

Where did the story come from?

The study was carried out by researchers from the EpidStat Institute in Michigan and DLW Consulting Services in Utah, both in the US, and was funded by the Egg Nutrition Center. This could be seen as a conflict of interest.

The study was published in the peer-reviewed Journal of the American College of Nutrition.

The news was greeted with enthusiasm and little criticism by the UK media. Most reported the study results reasonably accurately.

Both The Sun and the Daily Mirror described the modest 12% drop in relative risk as having "slashed" stroke risk, which is something of an exaggeration.

Although several reports included quotes from the Egg Nutrition Center, none pointed out that the centre had funded the study.

The Egg Nutrition Center is the self-styled "science and nutrition education division" of the American Egg Board (AEB), which is a trade association representing American egg farmers.

The Times' headline stated that eating eggs could cut chances of having a "fatal" stroke, but the study did not find a statistically significant difference in risk of fatal stroke from egg consumption.

What kind of research was this?

A meta-analysis is a good way of summarising the research on a topic; however it's only as good as the studies included. In this case, all were prospective cohort studies.

Cohort studies can find links between factors (egg consumption and heart disease or stroke) but cannot show that one factor causes another.

What did the research involve?

Researchers identified all prospective studies published up to August 2015, which looked at egg consumption by adults and either heart disease or stroke.

They pooled the results and looked to see whether high egg consumption compared to low egg consumption had any effect on these outcomes. They also looked for a "dose response" – a suggestion that risk went up or down in line with the number of eggs people ate each week.

Most of the studies classified high egg consumption as about an egg a day, and low egg consumption as less than two eggs a week.

Most, but not all, adjusted their figures to take account of confounding factors that can affect risk of heart disease and stroke, such as:

weight

age

sex

smoking history

exercise

(in a few cases) how healthy participants' diet was overall

The researchers did standard tests to look for publication bias and to see whether the summary results were overly affected by one or more studies.

What were the basic results?

People whose egg consumption was high were no more or less likely to get heart disease (summary relative risk estimate (SRRE) 0.97; 95% confidence interval (CI) 0.88 to 1.07) than people whose egg consumption was low. This result was based on seven studies including 276,000 people.

However, people who ate an egg per day were 12% less likely to have a stroke than people who ate less than two eggs per week (SRRE 0.88, 95% CI 0.81 to 0.97). This was based on seven studies including 308,000 people.

The researchers found no sign that the stroke risk decreased in proportion to the number of eggs eaten.

How did the researchers interpret the results?

The researchers concluded: "consumption of up to one egg daily may contribute to a decreased risk of total stroke [all types of stroke] and daily egg intake does not appear to be associated with risk of coronary heart disease."

Conclusion

This research broadly supports previous studies in this area, which suggest eating eggs does not increase the chances of getting heart disease or stroke. It raises the possibility that eggs may decrease the risk of having a stroke, but there are limitations to the study, meaning this result may not be reliable.

It's interesting that researchers did not find a "dose response" between stroke risk and the number of eggs eaten. Usually, if something is having an effect on the chances of getting a condition, you can see a linear pattern – having more of that food or treatment increases or decreases chances of the disease, perhaps up to a certain point. But in this case, you can't see any clear pattern.

Studies that identify just one factor – in this case people's egg consumption –without balancing that with information about their overall diet and lifestyle, may find false associations that are actually explained by other factors. For example, people who eat eggs may be more likely to eat a generally healthy diet, or to exercise more, both of which would decrease the chances of stroke.

Another factor to be aware of is that the 12% risk reduction is quite small, and the confidence interval comes fairly close to the point at which the result is no longer statistically significant. This means it is close to the margin of error, so could be down to chance or a blip in the data.

It is important to remember to eat a balanced diet, rather than just assuming one type of food is best. There's a big difference between eating a daily boiled or poached egg with wholegrain toast and spinach, or eating an egg as part of a daily fry-up full of salt and fat.

"Women have caught up with men in the amount of alcohol they drink," The Guardian reports.

A survey of data from around the world suggests the gap between men and women is closing rapidly when it comes to alcohol use and subsequent alcohol-related harms.

Researchers looked at 68 studies from across the world studying people born from 1891 to 2000 to examine changing trends in alcohol use in men and women.

In the early 1900s, men were twice as likely as women to drink alcohol and three times more likely to experience alcohol-related problems. Now, there is far less of a difference, so the genders have very nearly equalised.

Despite the many suggestions mooted in the media – such as the influence of "90s ladette culture" – the study did not investigate the reasons behind the rise.

The authors suggest the findings indicate the need to particularly focus on young women to reduce the impact of alcohol use and related harms.

Women are more vulnerable to the harmful effects of alcohol because of a number of factors, such as the fact it takes longer for their bodies to break down alcohol.

To keep health risks to a low level, both men and women are advised to drink no more than 14 units a week.

Where did the story come from?

The study was carried out by researchers from the Australian NHMRC Centre of Research Excellence in Mental Health and Substance Use at the University of New South Wales, Australia, and Columbia University Mailman School of Public Health in the US.

It was funded by the Australian Government under the Substance Misuse Prevention and Service Improvements Grant Fund and a National Health and Medical Research Council Centre of Research Excellence Grant. The authors declare no competing interests.

The media generally reported the story accurately. However, despite many suggestions provided by the media and independent experts, the study did not investigate why these trends have changed.

One hypothesis put forward by the researchers is that more women are now working than 50 years ago, so they have an independent income. This may mean they are free to socialise as they wish without having to rely on their partner.

What kind of research was this?

This systematic review and meta-analysis aimed to summarise published literature on changes across time of male-to-female ratios in key indicators of alcohol use and related harm.

While meta-analyses are a useful way of pooling research in an area, they are only as good as the individual studies included.

In this case, 68 studies were included in total:

48 repeated cross-sectional studies

19 single cross-sectional studies

1 longitudinal study

These study designs can provide observational information from a single point in time or show how things have changed over time, but they can't provide answers to explain the trends.

There may also be some inaccuracies in terms of how representative the populations were or the information on frequencies of alcohol use.

What did the research involve?

The review used accepted quality standards for performing a systematic review. Studies including regional or nationally representative populations were identified.

Separate data for males and females was given on at least one of the following key indicators of alcohol use and harms:

lifetime or current alcohol use disorder – for example, dependence

alcohol-related problems – for example, drunkenness or other negative consequences

alcohol-related treatment

seeking stages in the alcohol use and related problems cycle – for example, onset of use or transition from use to disorder

heavy episodic or binge drinking

Researchers pooled the data from 68 relevant international studies published between 1980 and 2014, including a comparison of male and female drinking patterns.

The studies included collected data between 1948 and 2014, and included 4,426,673 people born as far back as 1891 and up to 2000. Of those, just over a third each were from North America and Europe.

The births were grouped into five-year cohorts from 1891 to 2000, except for the first (1891-1910) and last (1991-2000), generating 1,568 sex ratios. The study quality was assessed by two independent moderators.

The male-to-female ratios were calculated for three broad categories:

any alcohol use

problematic alcohol use

alcohol-related harms

The meta-analyses resulted in pooled sex ratios within these three categories for each birth cohort.

What were the basic results?

The pooled data showed that the gap between men and women consistently closed across all three categories of any alcohol use, problematic alcohol use and alcohol-related harms:

alcohol use – the sex ratio of men to women was 2.2 (95% confidence interval [CI] 1.9 to 2.5) in the 1891-1910 birth cohort, indicating men were two times more likely to report any alcohol use compared with their female counterparts; this decreased to a low of 1.1 (95% CI 1.1 to 1.2) for those born between 1991 and 2000

problematic alcohol use – the sex ratio decreased from 3.0 (95% CI 1.5 to 6.0) in the 1891-1910 cohort to 1.2 (95% CI 1.1 to 1.4) in those born between 1991 and 2000

alcohol-related harms – the sex ratio decreased from 3.6 (95% CI 0.4 to 30.4) in the 1911-15 birth cohort (no earlier data) to 1.3 (95% CI 1.2 to 1.3) in those born between 1991 and 2000

For all three broad categories, sex ratio declined by 3.2% every five years across birth cohorts after accounting for potential bias. However, it was steepest in cohorts born from 1966 onwards.

How did the researchers interpret the results?

The researchers concluded that, "Alcohol use and alcohol use disorders have historically been viewed as a male phenomenon.

"The present study calls this assumption into question, and suggests that young women in particular should be the target of concerted efforts to reduce the impact of substance use and related harms."

They also said: "That the birth cohort effect on sex ratios has become more pronounced in these recent birth cohorts points to the value of continuing to focus research on adolescent and young adult sex-specific trends in substance use.

"Given that this young age group are relatively early in their alcohol use careers, these findings highlight the importance of further tracking young male and female cohorts as they age into their 30s, 40s and beyond."

Conclusion

This review provides support that the male-female gap in indicators of alcohol use and related harms has been closing. This is more evident in young adults, and has changed quicker in more recent years.

While the study provides evidence of a continuing trend, there are some key limitations.

The review can provide observations of trends over time, but cannot tell us the reasons behind the closing of the alcohol use gap.

It did not examine, for example, whether the changes in sex ratios in alcohol use and alcohol-related harms are the result of a fall in prevalence among men or a rise in women.

The authors speculated about some of the reasons behind this narrowing sex difference.

They suggested it could be down to the female gender role changing over time – for example, the increasing participation of women in the labour force, better education, and increased age of first marriage.

They also suggested broader social, cultural and economic changes might be involved.

Another important limitation is that these estimates may be imperfect. The studies included were all assessed for quality, though are likely to have varied widely in their inclusions, methods and follow-up.

For example, the majority of studies were from the US and Europe, but we can't say they'd be applicable to all populations.

The questions used to assess alcohol use and problems are also likely to have varied widely across studies, and across the century that the study covered.

Participants may also not have been fully reliable in their responses – which again could have differed over the years.

For example, it's possible that women in the earlier part of the 1900s may have been less willing to report excess alcohol consumption because of social perception, even if they did drink higher quantities of alcohol.

Overall, this is a good data set and likely to be the best we can get on this question, but the data still really needs to be considered to be estimates and not definite figures.

To keep health risks from alcohol to a low level if you drink most weeks:

men and women are advised not to drink more than 14 units a week on a regular basis

spread your drinking over three or more days if you regularly drink as much as 14 units a week

if you want to cut down, try to have several drink-free days each week

"Drinking more than two sugary or artificially sweetened soft drinks per day greatly increases the risk of diabetes, research has shown," The Guardian reports.

The research was a Swedish cohort study of sweetened drink consumption over the past year for people diagnosed with type 2 diabetes. They also looked at people with an uncommon form of diabetes known as latent autoimmune diabetes in adults (LADA) which shares features with type 1 and 2 diabetes.

Both groups were then compared with a diabetes-free control group.

Drinking more than two sweetened drinks per day was linked with being roughly twice as likely to have diabetes.

For type 2 diabetes the link was similar when separately analysing sugary and diet drinks. The link with LADA was a little weaker and did not stand up to statistical significance when separately analysing sugary and artificially-sweetened drinks.

However, this study cannot prove that sweetened drinks alone have directly caused these conditions. Other unhealthy lifestyle factors like smoking and poor diet in general were also linked with the two forms of diabetes.

Also, one of the hallmark symptoms of diabetes is increased thirst so it could be possible that in some cases the diabetes came first and was then followed by increased consumption of sweetened drinks.

These uncertainties aside, the results broadly support our understanding of the risk factors for diabetes, which also apply to several other chronic diseases.

Where did the story come from?

The study was carried out by researchers from the Karolinska Institutet, Stockholm and other institutions in Sweden and Finland. Funding was provided by the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, AFA Insurance and the Swedish Diabetes Association.

All the media reports mentioned two drinks per day. The significant links were actually for more than two drinks per day – for example, two-and-a-half or three.

There were no links for two or fewer drinks of any type. In any case, with food frequency questions there is the chance that estimates on portion size or frequency may be inaccurate.

What kind of research was this?

This was a case-control study within a population-based Swedish cohort study that aimed to see whether consumption of sweetened drinks was associated with risk of a rare form of diabetes called latent autoimmune diabetes in adults (LADA).

LADA has features of type 1 diabetes, where the body's own immune cells destroy the insulin-producing cells in the pancreas. But unlike type 1 diabetes, which normally develops in childhood, in LADA the cell destruction is much slower.

Also, the condition often develops later in life and shares many features with type 2 diabetes. For example, the person doesn't always need treatment with insulin straight away. This study reports that in the Swedish diabetes registry, LADA accounts for 5% of all cases.

The researchers compared drink consumption between cases with LADA or conventional type 2 diabetes and diabetes-free controls. The difficulty with this study design is that it's always going to be difficult to prove that a single factor, such as sweetened drinks, is definitely the cause of the condition.

What did the research involve?

The study used data from the population-based cohort study ESTRID (Epidemiological Study of Risk Factors for LADA and Type 2 Diabetes) which started in 2010.

This study invited people with LADA or Type 2 diabetes from the Swedish diabetes registry to take part, along with a random selection of people aged 35 or over who were free from diabetes to act as controls.

Participants were set to be recruited in a ratio of four people with type 2 diabetes and six controls for every one person with LADA.

All people with diabetes were diagnosed by a doctor. There are said to be no definite criteria for LADA diagnosis, but the study used criteria in line with other literature.

Participants completed a health and lifestyle questionnaire. This included information on weight and height, physical activity, smoking, alcohol intake, family history of diabetes and educational level.

They also completed a 132-item food frequency questionnaire. Participants were asked to report their normal food consumption in the preceding year. Three questions asked about intake of sweetened drinks:

cola

diet cola

other diet soft drinks/soda (for example diluted syrups)

They were asked to report the number of 200ml servings per day or per week. Questions on fruit juice weren't analysed in the study.

The researchers analysed the difference in sweetened drink consumption between cases and controls, adjusting for the other confounders.

What were the basic results?

Data was available for 1,136 people with type 2 diabetes, 357 people with LADA, and 1,371 diabetes-free controls.

Average age was 59 for people with LADA and controls, and 68 for those with type 2 diabetes.

Just under two-thirds of all people reported consuming sweetened (including artificially sweetened) drinks.

In general they found that consumption of sweetened drinks was linked with higher body mass index (BMI) and other poor lifestyle factors like smoking, low physical activity and consumption of processed meat and sugary foods.

In adjusted analyses, people drinking more than two servings of any sweetened drinks a day had almost doubled odds of LADA compared with non-consumers (odds ratio [OR] 1.99, 95% confidence interval [CI] 1.11 to 3.56). Each extra daily serving was linked with 15% increased risk (OR 1.15, 95% CI 1.02 to 1.29).

For type 2 diabetes, the link was a little stronger. More than two servings a day was linked with more than twice the odds of type 2 compared with non-consumers (OR 2.39, 95% CI 1.39 to 4.09), and each extra daily serving conferred a 20% increased risk (OR 1.20, 95% CI 1.07 to 1.34).

When separately analysing both sugar-sweetened and artificially-sweetened drinks, the findings were similar and still significant for type 2 diabetes. However, for LADA all links fell short of statistical significance on separate analysis.

Drinking two or fewer drinks per day – either sugar-sweetened or artificially-sweetened drinks – was not linked with either LADA or type 2 diabetes.

Conclusion

This study primarily aimed to see if consuming sweetened drinks was associated with the rarer condition of LADA, as it is with type 2 diabetes.

The researchers found that having more than two drinks per day was linked with increased odds of both conditions – though the link with LADA was a little weaker and not statistically significant when separately analysing diet and sugary drinks.

They also found that high BMI and other poor lifestyle choices were also linked with the conditions.

The findings generally support what is understood about type 2 diabetes, that high sugar intake, poor diet, low activity and high BMI increase risk. They similarly show that this is also likely to be the case with this rarer variant of the condition.

There are a couple of points to note:

This study design cannot prove that sweetened drinks are the direct cause of diabetes in these people. It is likely that high consumption of sweetened drinks is part of a wider picture of generally poor lifestyle habits. Though the researchers have adjusted their analyses for confounding factors, it is difficult to fully account for each health and lifestyle variable that could be having an influence.

The results are based on a food frequency questionnaire assessing intake over the past year. Though this is the best way you can look at this, it may not be entirely accurate – particularly when questioning regular portion size – or reflect longer term patterns over the course of the person's lifetime.

Several of these analyses deal with small numbers. For example, only 14 people with LADA drank more than two servings of diet drinks a day. Analyses based on small numbers are generally less reliable than those based on larger numbers of people.

This is a Swedish cohort. Lifestyle and environmental differences may mean the study is not completely representative of the UK population.

One expert from the University of Cambridge also considers another possibility that increased drink consumption could be due to increased thirst before diabetes is diagnosed – that is, the study can't rule out that this finding could be a symptom rather than a cause of diabetes.

The researchers did try and take account of consumption of water and other drinks as a general marker of thirst, but this is still a possibility the study design can't rule out.

Nevertheless, the findings support current understanding of the risk factors for diabetes, which apply to several other chronic diseases.

"Coffee really can help to prevent dementia: Just two cups a day 'cuts the risk of developing it by 36 per cent','' the Mail Online reports. But if you look closely at the research behind this report, the results are of borderline significance, meaning it is likely they were influenced by chance.

Researchers in the US found that postmenopausal women who consume an average of 261mg of caffeine a day (the equivalent of two to three cups of coffee) are at lower risk of cognitive impairment or probable dementia, than those who consume lower levels of caffeine.

The study followed 6,467 women for up to 10 years. Those consuming more caffeine were found to be at lower risk of having problems with cognitive functioning.

However, caffeine consumption was based on self-report and decaffeinated drinks were not specified, it was presumed all coffee, tea and cola drinks were caffeinated.

In addition, the results were modest to say the least. While researchers estimated the preventative effect was 26% (not 36% as widely reported in the media), according to the maths used by the researchers, the actual figure could be as low as 1%.

Where did the story come from?

The study was carried out by researchers at the University of Wisconsin-Milwaukee, Wake Forest School of Medicine, the Health Partners Institute for Education and Research in Minnesota, and Harvard Medical School, all in the US.

The study was funded by the National Heart, Lung and Blood Institute, at the National Institutes for Health, US. The authors do not report any sources of conflict.

The quality of the UK media's reporting of the study was poor. Firstly, most of the headlines, such as the Mail's "Coffee really can help to prevent dementia," overstated the implications of the study's results.

Secondly, nobody highlighted that the main result in terms of dementia prevention only barely scraped the level required for statistical significance.

Finally, and most importantly, all of the UK media's sources reported a factual inaccuracy. The actual reduction in terms of hazard ratio was 26% not 36%.

The inaccuracy appears to originate with a press release from the EurekAlert! science news service. This suggests no UK media source bothered to read the actual study (which to be fair to EurekAlert! was linked to in its article) and instead just used the press release.

What kind of research was this?

This was a prospective cohort study which aimed to assess the relationship between caffeine intake and overall incidence of probable dementia or cognitive impairment in postmenopausal women. Previous research in animals has suggested a protective effect of caffeine and other components in coffee on brain function.

The researchers used data from a long running randomised controlled trial in the US called the Women's Health Initiative. Women aged 65 to 80 had been randomised to take oestrogen tablets or placebo between 1995 and 1999. They were followed up annually for up to 10 years.

As this was a cohort study using data from the trial, it can only show a link between one factor – in this case caffeine intake – and another – dementia and cognitive impairment. It cannot prove caffeine intake lowered the risk of dementia or cognitive impairment.

What did the research involve?

Researchers looked at data from 6,467 women who had provided self-reported caffeine data within six months of starting the study and had at least one follow-up cognitive assessment.

Global cognitive function was assessed annually by trained, certified technicians and interviewers using the 100-point Modified Mini Mental State (3MS) exam until 2007. Annual assessment after 2007 was done by the 40 point Telephone Interview for Cognitive Status-modified (TICSm).

Both the 3MS and the TICSm are well validated methods of assessing and measuring cognitive abilities.

Caffeine intake was based on self-report at the start of the study using a food frequency questionnaire (FFQ). Caffeine intake was estimated from questions on coffee, tea, and cola beverages, including frequency and serving size. It was presumed that intake of these drinks were of the caffeinated form as there was no specific question asking about decaffeinated forms.

The data was analysed according to caffeine intake and the time until incidence of probable dementia or cognitive impairment. The results were adjusted to take into account risk factors including:

age

education

body mass index

hormone therapy

race

sleep quality

depression

hypertension

prior cardiovascular disease

diabetes

smoking

alcohol consumption

What were the basic results?

In a sample of generally healthy postmenopausal women, during the 10 years of follow-up, 209 women received a classification of probable dementia and 179 of mild cognitive impairment.

Women who drank more than 172mg of caffeine per day (equivalent to just under two cups of coffee) had a 26% lower risk of probable dementia than those who drank less (adjusted hazard ratio (HR) 0.74, 95% confidence interval (CI) 0.56 to 0.99). As mentioned this result is borderline statistically significant.

They were also 26% less likely to have either probable dementia or mild cognitive impairment (HR 0.74, 95% CI 0.60 to 0.91).

The average amount of caffeine consumed in the women above the 172mg cut-off was 261mg, equating to about three cups of coffee or five cups of tea. The average amount consumed below the cut-off was 64mg.

How did the researchers interpret the results?

The researchers concluded that they showed a "lower risk of probable dementia or global cognitive impairment incidence in women with higher caffeine consumption, which are generally consistent with the literature."

Although more studies are needed to verify the consistency of reports, given that caffeine intake is easily modifiable, it is important to quantify its relationship with cognitive health outcomes not only from preventative stand point but also to better understand the underlying mechanisms and their involvement in dementia and cognitive impairment.

They further add "given that Alzheimer's disease prevalence is expected to quadruple by 2050, even a small reduction in age-related cognitive impairment or dementia burden would thereby have significant public health implications."

Conclusion

This study suggests there is a link between self-reported caffeine consumption and risk of developing probable dementia or some kind of cognitive impairment.

The findings could be important in leading to more research to investigate the mechanisms by which caffeine might provide protection against dementia and cognitive impairment. The hope being that such investigation may eventually lead to new forms of drug treatments.

However, there are several limitations of the study, including:

The level of caffeine was self-reported and may be inaccurate, particularly as it was presumed the reported intake of coffee, tea and cola were all caffeinated, which may not be the case.

As the actual levels of caffeine were not measured in the study, it may have been another component in coffee, tea of cola that was having a positive effect on the cognitive ability of the women.

The women in the sample were mostly white and generally highly educated and may not be representative of the general population which may have had an impact on the cognitive functioning scores.

Although some confounding factors were adjusted for, some were not, for example other aspects of women's diets and family history of dementia.

Breaking down level of caffeine consumed into more than two groups would have been useful to observe if cognitive function improves with caffeine consumed or if there is an optimum level of caffeine consumption somewhere in the middle.

Finally, the measures of cognitive function were not consistent throughout the study and therefore comparing women assessed using different instruments may lead to over- or under-estimation of cognitive impairment or probable dementia, causing inaccuracies in the conclusions.

Overall, it cannot be said that women consuming more caffeine are at a lower risk of developing cognitive impairment or probable dementia. More research is needed to identify whether there are mechanisms by which caffeine may be a protective factor in cognitive functioning.